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GI part 2

Kyha Avery Pathophysiology Resp Therapy Inglés 65 fichas

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  1. 1What are accessory organs to the digestive system?Liver, gallbladder, & pancreas
  2. 2What is the largest visceral organ in the body?Liver
  3. 3How many lobes does the liver have?2 large lobes (R lobe & L lobe)
    2 small lobes (caudate & quadrate)
  4. 4How much CO does the liver recieve?25%
  5. 5What are functional units of liverLobules
  6. 6Where does the liver receive blood from?Dual blood supply - venous portal supply & arterial blood supply
  7. 7Explain how the liver receives venous blood1.) Venous blood via hepatic portal vein comes from digestive tract & GI organs
    2.) Carries nutrients & toxic materials
    3.) Supplies 75% of O2 to liver
    4.) Venous outflow carried by hepatic veins → empties into vena cava
  8. 8How much blood can the liver hold?Liver can hold 500 – 1000mL of blood
  9. 9What can cause an increase in accumulation of blood in the liverRight heart failure → ↑ vena cava pressure → ↑ accumulation of blood in liver
  10. 10Metabolic Functions of the LiverProduces bile
    Metabolizes drugs and hormones
    Eliminates bilirubin
    Synthesizes proteins, glucose, clotting factors (including albumin)
    Stores vitamins and minerals
    Changes ammonia to urea
    Converts fatty acids to ketones
    Degrades excess nutrients
  11. 11Why does the liver secrete bile? How much does it secrete?For digesting fat, absorbing fats and vitamins from the intestine. Produces 500-600 mL/day.
  12. 12What does bile contain?Water, bile salts, bilirubin, cholesterol, other metabolism by-products
  13. 13What do bile salts aid in?Emulsifying fats
  14. 14What is Cholestasis?decrease in bile flow → accumulation of bilirubin, cholesterol and bile salts in blood
  15. 15What are symptoms of Cholestasis?dark urine, jaundice, steatorrhea (fat within feces), itchy skin
  16. 16What is bilirubin?Bilirubin = final product of breakdown of heme (from old RBCs)
    eliminated through bile → small intestine → feces
  17. 17What is Jaundice? How is it caused?1.) Results from high levels of bilirubin in blood
    2.) Causes yellowish discoloration of skin and deep tissues
    3.) Occurs when imbalance between synthesis and clearance of bilirubin
  18. 184 causes of Jaundice1.) Excessive destruction of RBCs
    2.) Impaired uptake of bilirubin by hepatocytes
    3.) Decreased conjugation of bilirubin
    4.) Obstruction of bile flow (cholestasis)
  19. 19What is Hepatitis?liver inflammation caused by hepatotropic viruses
  20. 20What are the different types of Hepatitis? How do they differ?Hepatitis A, B, C, E (all cause acute hepatitis) but differ in:
    1.) mode of transmission
    2.) Incubation period
    3.) Mechanism, degree and chronicity of liver damage
    4.) Ability to evolve to carrier state
  21. 21What are 2 mechanisms of liver injury?Direct cellular injury – caused by virus in cell
    Immune response against viral antigens
  22. 22What does Hepatitis cause cells to do?Hepatitis causes cell to express surface antigen – recognized by T-cells to trigger cytotoxic killing & apoptosis
  23. 23Common Symptoms & Signs of Hepatitis1.) hepatomegaly
    2.) ↑ transaminase in blood (as damage progresses) – AST & ALD
    3.)Jaundice – bilirubin in blood stream (damage to bile ducts causes leaking)
  24. 24Hepatitis ASmall unenveloped RNA virus
    Almost always acute (doesn’t progress to chronic hepatitis)
  25. 25Transmission of Hep ATransmission: ingestion (fecal-oral route)
  26. 26Pathophysiology of Hep APathophysiology: replicates in liver; excreted in bile; shed in stool
  27. 27Dx & Tx of Hep Aserologic testing (IgM anti-HAV)
    Prevention: Hep A vaccine
    Tx: supportive care
  28. 28Hep BDNA virus. Can be acute or chronic
  29. 29Hep B transmissionparenterally
  30. 30Hep B Dx & Txserologic testing (HBsAg)
    Prevention: Hep B vaccine
    Tx: supportive care; liver transplant if fulminant disease
  31. 31Hep CRNA virus. Acute & Chronic types
  32. 32How is Hep C transmittedBlood, needle-sharing, sex
  33. 33How to Dx & treat Hep CDx: PCR assay for HCV RNA
    Prevention: avoid high-risk behavior (no vaccine)
    Tx: antiviral therapy; liver transplant (leading reason for liver transplant)
  34. 34Where is alcohol mostly metabolized?In the liver
  35. 35How is acetaldehyde made?ETOH → ADH → acetaldehyde
  36. 36What is acetaldehyde?Acetaldehyde is a toxic & reactive molecule
    Leads to radical formation (ROS)
    Impedes mitochondrial electron transport system
  37. 37Acetaldehyde dehydrogenase (ALDH) breaks down what into whatADH → acetate
  38. 38What are 3 stages in ETOH Liver Disease?1.) Fatty Liver Disease
    2.) Alcoholic Hepatitis
    3.) Alcoholic Cirrhosis
  39. 39Explain fatty liver diseaseAccumulation of fat in hepatocytes – steatosis
    Liver turns yellow and enlarges
    Reversible if alcohol intake stops
  40. 40Explain Alcoholic hepatitisCommon in binge drinkers
    Inflammation and necrosis of liver cells
    Hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites, liver failure
  41. 41Explain Alcoholic CirrhosisEnd-stage liver disease
    Fine, uniform nodules on surface of liver
    Nodules grow as disease progresses → compress hepatic veins → portal hypertension and cholestasis
  42. 42What is considered end-stage chronic liver disease?Cirrhosis
  43. 43What is Cirrhosis? What is it caused by?Function liver tissue replaced by fibrous tissue
    Caused by multiple disease processes
  44. 44Pathophysiology of CirrhosisHepatic fibrosis
    Regenerative nodules – classic sign of cirrhosis
    Between nodules is fibrotic tissue and collogen
    Compresses portal vein (portal hypertension) → fluid into peritoneal cavity → ascites
    Hepatoportal shunt
  45. 45Complications of CirrhosisPortal hypertension → ascites, varices
    Hepatic encephalopathy (increase in ammonia blood levels)
    Jaundice
    Coagulopathy
  46. 46Signs & Symptoms of Cirrhosis (this is more w/o hx of ETOH)1.) Palpable firm liver
    2.) Weight loss
    3.) Anorexia
  47. 47How to Dx Cirrhosis1.) Liver blood test (AST,ALT)
    2.) Coagulation Tests
    3.) Imagining to asses for nodules & fibrosis
    4.) Liver biopsy if you can't tell by imaging
  48. 48How to Tx Cirrhosis1.) Supportive care
    2.) Stop injurious agent
    3.) TIPS if portal hypertension is refractive to other tx
  49. 49What is portal hypertension?Elevated pressure in the portal vein
  50. 50What causes portal hypertensionCause: increased resistance to hepatic blood flow
    1.) Thrombosis
    2.) compression due to cancer growth
    3.) Severe right-sided heart failure
    4.) Fibrosis from cirrhosis (major cause)
  51. 51Complications of portal hypertension1.) Ascites
    2.) Splenomegaly
    3.) Hepatic encephalopathy
    4.) Formation of portosystemic shunts → esophageal varices
  52. 52What is in the hepatobiliary system?Gallbladder; hepatic duct; common bile duct
  53. 53What is the Gallbladder & what does it do?Gallbladder is pear-shaped muscular sac
    Stores and concentrates bile
  54. 54What happens when food enters the intestine?triggers gallbladder to contract and open the sphincter of bile duct → moves bile into the duodenum
  55. 55What is Cholelithiasis? What is it caused by?Gallstones. Caused by precipitation of substances of bile (usually cholesterol & bilirubin)
  56. 56What are gallstones formed from?Formed from:
    Abnormalities in the composition of bile (↑ cholesterol)
    Stasis of bile
  57. 57Signs & symptoms of Gallstonesindigestion; jaundice; pain (URQ) with abrupt onset
  58. 58Dx & Tx of GallstonesDx: U/S
    Tx: laparoscopic cholecystectomy
  59. 59What kind of organ is the pancreas?endocrine and exocrine
  60. 60What is the pancreas' endocrine function?secrete digestive enzymes into ducts that empty into the bile duct at the hepatopancreatic ampulla and empties into duodenum
  61. 61What do pancreatic secretions contain? When do the secretions become active?Proteolytic enzymes; pancreatic amylase; lipases
    Don’t become active until in the intestine
  62. 62What is Acute PancreaticReversible inflammation of the pancreatic acini (cells of the pancreas’ lobules).
    Caused by the premature activation of the pancreatic enzymes
  63. 63Pathophysiology of Acute Pancreatitispremature activation → autodigestive injury → damage tissue activate inflammatory cascade → produce cytokines → inflammation and edema
  64. 64Signs & Symptoms of Acute Pancreatitistachycardia; hypotension; ↑ C-reactive protein on labs
  65. 65Dx & Tx of Acute PancreatitisDx: need two of the three features (abdo pain; ↑ serum amylase/lipase; imaging showing acute pancreatitis
    Tx: supportive – fluid resuscitation, pain control and nutritional support
    Avoid stimulation for secretion of enzymes (withhold food)

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Resp Therapy Pathophysiology Fichas sobre GI part 2, creado por Kyha Avery el 31/10/2023.
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Kyha Avery
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